At these stages, RA is produced by RALDH2 in the newly-formed somites and the rostral presomitic mesoderm. It has been shown, both in avian models and mouse mutants deficient for RA synthesis, that retinoid signaling is indispensable for controlling neurogenesis and patterning in the developing spinal cord, and regulating somite size and left-right symmetry [Diez del Corral et al., 2003; Diez del Corral and Storey, 2004; Duester, 2007; Maden, 2006; Reijntjes et al., 2005; Ribes et al., 2009; Vermot et al., 2005a; Vermot and Pourquie, 2005; Wilson and Maden, 2005]. In these processes, RA appears to antagonize posterior signals, including Wnt3a and FGF8, required for the maintenance of an undifferentiated 'stem' zone within the embryonic tail bud. Rar single or compound knockout mice have not been found to display such defects in spinal cord neurogenesis or mesodermal segmentation (for details and references, see accompanying review by [Mark et al., 2009]). This could be because RA has critical functions in the transition region between the posterior 'stem' zone and the differentiating tissues, where Rarb and Rarg (as well as Rara) would
